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David J. Boarini, Neal F. Kassell, James A. Sprowell, Julie J. Olin, and Hans C. Coester

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole.

In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

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David J. Boarini, Neal F. Kassell, Julie J. Olin, and James A. Sprowell

✓ Prostacyclin has strong vasodilating and antiplatelet properties. This study was performed to investigate its potential for producing profound intraoperative hypotension. Five dogs were anesthetized with morphine, nitrous oxide, and oxygen, paralyzed with pancuronium, and ventilated to a PaCO2 of 40 torr. Mean arterial blood pressure (MABP) was lowered to 40 mm Hg with an intravenous infusion of prostacyclin in 0.05 M Tris buffer (average rate of infusion 3 ± 1 µg/kg/min). Blood flow was determined using the radioactive microsphere technique. Measurements were made before and after 20, 40, and 60 minutes of hypotension; and after a 40-minute recovery period. Infusion of prostacyclin reduced MABP 63% while increasing heart rate 51%. Tachyarrhythmias occurred in all dogs, and cardiac index decreased 18%. Myocardial blood flow decreased an average of 29%, cerebral blood flow decreased 30%, cerebellar blood flow decreased 18%, and blood flow in the brain stem and spinal cord was unchanged. Cerebral metabolic rate of oxygen, determined by measuring the oxygen content of the sagittal sinus, was unchanged. Hypotension was easily induced and maintained using prostacyclin, without apparent tachyphylaxis. However, the cardiac changes caused by this drug are more severe than those accompanying hypotension induced by most other agents, and may represent a serious contraindication to its clinical use.

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Neal F. Kassell, David J. Boarini, Julie J. Olin, and James A. Sprowell

✓ In six dogs anesthetized with halothane and nitrous oxide, mean arterial pressure (MAP) was lowered to 40 mm Hg for an average of 90 minutes by intravenous infusion of adenosine. The hypotensive effect of the adenosine was potentiated by administering dipyridamole to block its intravascular inactivation. Blood flow to the brain, spinal cord, heart, kidneys, and skeletal muscle was measured six times in each animal using the radioactive microsphere technique. Determinations were made before, during, and 30 minutes after the hypotensive period.

During the hypotensive period, MAP was decreased 61% and was related to a proportional decrease in peripheral vascular resistance. Cardiac index decreased 14%. Total cerebral blood flow (CBF) decreased an average of 28% and cerebral vascular resistance decreased 53%. The reduction in CBF was heterogeneous; the cerebral cortex and corpus callosum were most affected and the brain stem least affected. No change occurred in the cerebral metabolic rate of oxygen usage (CMRO2). Left ventricle flow increased 147% and right ventricle flow increased 271%. Blood flow to the kidneys decreased 70%, and to the liver decreased to 6% of control. Jejunum blood flow increased 138% during recovery, while stomach flow varied but showed no statistical change. There was no tachyphylaxis, rebound hypertension, or toxicity associated with the adenosine-induced hypotension. These properties suggest that adenosine may be a useful agent for inducing arterial hypotension in neurosurgical patients.

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Neal F. Kassell, David J. Boarini, James A. Sprowell, and Julie J. Olin

✓ The purpose of this study was to compare the behavioral, hematological, and biochemical effects of profound arterial hypotension induced by adenosine potentiated with dipyridamole with those of hypotension induced by trimethaphan camsylate or sodium nitroprusside. Twenty dogs were anesthetized with halothane and nitrous oxide, paralyzed with pancuronium, and ventilated to an arterial pCO2 of 40 torr. Arterial pressure and heart rate were monitored continuously. The animals were divided into four groups of five dogs each. The first group served as controls, while in the remaining groups the mean arterial pressure (MAP) was lowered to 40 mm Hg with adenosine/dipyridamole, trimethaphan, or nitroprusside for 1 hour, following which the animals were allowed to recover from the anesthetic and observed for 48 hours. Determinations of arterial blood gases and hematological and biochemical parameters were made immediately prior to and at the completion of the 1-hour hypotensive period and 48 hours later.

Reduction of MAP to 40 mm Hg was readily achieved with adenosine/dipyridamole. There was no tachyphylaxis to this drug, and arterial pressure promptly returned toward control levels without overshoot after the infusion was discontinued. In contrast, hypotension of this degree could be produced only with toxic doses of nitroprusside. Trimethaphan was more effective in producing hypotension than nitroprusside, but the dose required was extremely variable, and prolonged intervals were required for pressure to return toward normal after the agent was stopped. The control animals and those that received adenosine/dipyridamole recovered promptly from the anesthetic and were neurologically intact. The animals that received trimethaphan recovered more slowly but were neurologically normal within 12 hours. All of the animals that received nitroprusside died without recovering from the anesthesia. Aside from a mild transient metabolic acidosis and transient elevation of blood urea nitrogen and creatinine in the dogs that received adenosine/dipyridamole or trimethaphan, no specific cardiovascular, hematological, hepatic, or renal toxic effects were noted. Evidence of fatal cyanide toxicity was present in the nitroprusside group.

These data suggest that hypotension using adenosine/dipyridamole is readily induced, maintained, and reversed, and is not associated with any apparent hematological, or biochemical evidence of toxicity. Further studies leading to a clinical trial of adenosine-induced hypotension appear to be indicated.